乐果亚长期暴露对大鼠肝脏氧化应激的影响

本试验旨在研究乐果(Dimethoate)对大鼠的毒性作用,探讨乐果中毒的氧化应激机制.将24只SD大鼠分成对照组和3个染毒组,分别以0、1、6、30 mg/kg体质量剂量灌服乐果,连续灌服30 d后,测定血浆和肝脏胆碱酯酶(ChE)活性及肝脏中超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、过氧化氢酶(CAT)活性和丙二醛(MDA)含量,并观察肝脏组织学和超微结构变化.结果显示,乐果染毒后大鼠血浆和肝脏ChE活性均极显著降低(P<0.01);大鼠肝脏SOD活性呈上升趋势,而GSH-Px、CAT活性随染毒剂量增加呈先下降后上升趋势;各染毒组肝脏MDA含量均呈上升趋势;组织学和超微结构检查显示肝细胞脂肪变性、凋亡等.结果表明.大鼠乐果持续染毒可以诱导机体脂质过氧化增强,并导致肝脏结构损伤,说明氧化应激在乐果的肝脏毒性中发挥重要作用.     

Effect of GABA on oxidative stress in the skeletal muscles and plasma free amino acids in mice fed high‐fat diet

Increased levels of plasma free amino acids (pFAAs) can disturb the blood glucose levels in patients with obesity, diabetes mellitus and metabolic syndrome (MS) and are associated with enhanced protein oxidation. Oxidation of proteins, especially in the muscles, can promote protein degradation and elevate the levels of pFAAs. Gamma‐aminobutyric acid (GABA), a food additive, can reduce high‐fat diet (HFD)‐induced hyperglycaemia; however, the mechanisms remain unclear. The aim of this study was to evaluate the effects of GABA on protein oxidation and pFAAs changes. One hundred male C57BL/6 mice were randomly divided into five groups that were fed with control diet, HFD and HFD supplied with 0.2%, 0.12% and 0.06% GABA in drinking water for 20 weeks respectively. HFD feeding led to muscular oxidative stress, protein oxidation, pFAA disorders, hyperglycaemia and augmented plasma GABA levels. Treatment with GABA restored normally fasting blood glucose level and dose‐dependently inhibited body weight gains, muscular oxidation and protein degradation. While medium and low doses of GABA mitigated HFD‐induced pFAA disorders, the high dose of GABA deteriorated the pFAA disorders. Medium dose of GABA increased the levels of GABA, but high dose of GABA reduced the levels of plasma GABA and increased the activity of succinic semialdehyde dehydrogenase in the liver. Therefore, treatment with GABA mitigated HFD‐induced hyperglycaemia probably by repairing HFD‐induced muscular oxidative stress and pFAA disorders in mice. Our data also suggest that an optimal dose of GABA is crucial for the prevention of excess GABA‐related decrease in the levels of pFAA and GABA as well as obesity.     

Effect of mercury chloride on oxidative stress and nuclear factor erythroid 2‐related factor 2 signalling molecule in liver and kidney of laying hens

This study investigated the effects of mercury chloride (HgCl₂) on the deposition of mercury (Hg), histopathology and oxidative stress in liver and kidney of laying hens. The gene expressions of antioxidant enzymes and nuclear factor erythroid 2‐related factor 2 (Nrf2)‐Kelch‐like ECH‐associated protein 1 (Keap1) were further studied to uncover the molecular mechanism. A total of 960 40‐week‐old Hyline brown laying hens were randomly allocated to five treatments with eight pens per treatment and 24 hens per pen. The hens were fed with five experimental diets containing graded levels of Hg at 0.270, 1.250, 3.315, 9.405 and 27.230 mg/kg respectively. Results revealed that both deposition of Hg and score of injury in liver and kidney were significantly increased as dietary Hg dosage up to 27.230 mg/kg diet. Deposition of Hg was positively related to score of injury in liver and kidney of laying hens. Besides, the activities of superoxidative dismutase (SOD), catalase (CAT), glutathione reductase (GR) and glutathione peroxidase (GSH‐Px), and glutathione (GSH) content all significantly decreased (p < 0.05), while malondialdehyde (MDA) content significantly increased (p < 0.05) after Hg exposure in liver and kidney of laying hens. In addition, positive relationships occurred between antioxidant enzyme activities and antioxidant enzyme gene expressions except between SOD activity and manganese superoxide dismutase (MnSOD) gene expression in liver. Meanwhile, Nrf2 gene expression was positively related to antioxidant gene expressions and negatively connected with Keap1 gene expression. Negative relationships occurred between Nrf2 and Keap1 protein levels in liver and kidney. In conclusion, Hg could dose‐dependently damage liver and kidney and induced hepatic and renal oxidative stress by means of suppressing Nrf2‐Keap1 signalling molecule in laying hens.